scholarly journals Influence of various treatment methods on the content of cytokines in saliva of patients with chronic sialadenitis

2018 ◽  
Vol 99 (4) ◽  
pp. 593-597
Author(s):  
S Z Aliev

Aim. Study of the main cytokines (interleukin-1β and -2, interferon γ) in the mixed saliva from patients with chronic sialadenitis on the basic and comprehensive treatment dynamically. Methods. During the period of 2014 to 2017 we performed examination and treatment of patients with salivary gland diseases. Out of them we defined a group with chronic non-specific sialadenitis including 45 patients seen in the clinic in exacerbation. Patients in the comparison group received basic treatment. Patients in the study group additionally to conventional treatment were administered local immunotherapy. Measurement of cytokine levels in the oral fluid was performed in 45 patients with chronic sialadenitis in exacerbation and in 10 practically healthy subjects. Results. The level of interleukin-1β in saliva was found to be significantly increased before treatment (p <0.05). After the treatment interleukin-1β level in saliva decreased in both groups but most significantly this parameter decreased in the study group. After including local immunocorrection into the treatment complex dynamic decrease of interleukin-2 to 14.7±0.4 pg/ml was registered, which apparently is associated with stabilization of immune processes in the oral cavity. After the treatment conducted according to traditional scheme in the comparison group the level of interferon γ in saliva increased to 7.2±0.2 pg/ml which is 1.1 times higher than before treatment. Conclusion. In patients with chronic sialadenitis in exacerbation the level of interleukin-1β statistically significantly increases by 1. times (p <0.05), interleukin 2 - by 2.1 times (p <0.05) and the level of interferon γ decreases by 1.4 times (p <0.05) which is indicative of immunological signs of inflammatory reaction; use of local immunocorrection leads to more prominent decrease of interleukin-1β (by 20.3 vs 16.2% in comparison group; p <0.05), interleukin-2 (by 38.8 vs 26.6%; p <0.05) and increase of interferon γ (by 21.2 vs 12.5% in comparison group; p <0.05).

1997 ◽  
Vol 239 (1) ◽  
pp. 273-278 ◽  
Author(s):  
Cécile Calleja ◽  
Claudine Eeckhoutte ◽  
Gilberte Larrieu ◽  
Jacques Dupuy ◽  
Thierry Pineau ◽  
...  

2020 ◽  
Vol 222 (6) ◽  
pp. 1051-1061
Author(s):  
Jing-sheng Lou ◽  
Jia-feng Wang ◽  
Miao-miao Fei ◽  
Yan Zhang ◽  
Jun Wang ◽  
...  

Abstract Background Lymphocyte activation gene 3 (LAG-3) is one of the immune checkpoint molecules, negatively regulating the T-cell reactions. The present study investigated the role of LAG-3 in sepsis-induced T-lymphocyte disability. Methods Mice sepsis was induced by cecal ligation and puncture (CLP). LAG-3 expression on some immune cells were detected 24 hours after CLP. LAG-3 knockout and anti–LAG-3 antibody were applied to investigate the effects on the survival, bacterial clearance. Cytokine levels, T-cell counts, and the presence of apoptosis (in blood, spleen, and thymus) were also determined. In vitro T-cell apoptosis, interferon γ secretion, and proliferation were measured. The expression of interleukin 2 receptor on T cells was also determined after CLP. Results LAG-3 was up-regulated on CD4+/CD8+ T, CD19+ B, natural killer, CD4+CD25+ regulatory T cells and dendritic cells. Both LAG-3 knockout and anti–LAG-3 antibody had a positive effect on survival and on blood or peritoneal bacterial clearance in mice undergoing CLP. Cytokine levels and T-cell apoptosis decreased in anti–LAG-3 antibody–treated mice. Induced T-cell apoptosis decreased, whereas interferon γ secretion and proliferation were improved by anti–LAG-3 antibody in vitro. Interleukin 2 receptor was up-regulated on T cells in both wild-type and LAG-3–knockout mice undergoing CLP. Conclusions LAG-3 knockout or anti–LAG-3 antibody blockade protected mice undergoing CLP from sepsis-associated immunodysfunction and may be a new target for the treatment.


Author(s):  
Annette Paschen ◽  
Ignacio Melero ◽  
Antoni Ribas

Resistance to immunotherapy is due in some instances to the acquired stealth mechanisms of tumor cells that lose expression of MHC class I antigen–presenting molecules or downregulate their class I antigen–presentation pathways. Most dramatically, biallelic β2-microglobulin (B2M) loss leads to complete loss of MHC class I expression and to invisibility to CD8+ T cells. MHC class I expression and antigen presentation are potently upregulated by interferon-γ (IFNγ) in a manner that depends on IFNγ receptor (IFNGR) signaling via JAK1 and JAK2. Mutations in these molecules lead to IFNγ unresponsiveness and mediate loss of recognition and killing by cytotoxic T lymphocytes. Loss of MHC class I augments sensitivity of tumor cells to be killed by natural killer (NK) lymphocytes, and this mechanism could be exploited to revert resistance, for instance, with interleukin-2 (IL-2)-based agents. Moreover, in some experimental models, potent local type I interferon responses, such as those following intratumoral injection of Toll-like receptor 9 (TLR9) or TLR3 agonists, revert resistance due to mutations of JAKs. Expected final online publication date for the Annual Review of Cancer Biology, Volume 6 is April 2022. Please see http://www.annualreviews.org/page/journal/pubdates for revised estimates.


1999 ◽  
Vol 86 (6) ◽  
pp. 2065-2076 ◽  
Author(s):  
Stephen K. Chapes ◽  
Steven J. Simske ◽  
Gerald Sonnenfeld ◽  
Edwin S. Miller ◽  
Robert J. Zimmerman

Sprague-Dawley rats were subjected to two 8-day spaceflights on the space shuttle. Rats housed in the National Aeronautics and Space Administration’s animal enclosure were injected (iv or sc) with pegylated interleukin-2 (PEG-IL-2) or a placebo. We tested the hypothesis that PEG-IL-2 would ameliorate some of the effects of spaceflight. We measured body and organ weights; blood cell differentials; plasma corticosterone; colony-forming units (macrophage and granulocyte macrophage); lymphocyte mitogenic, superantigenic, and interferon-γ responses; bone marrow cell and peritoneal macrophage cytokine secretion; and bone strength and mass. Few immunological parameters were affected by spaceflight. However, some spaceflight effects were observed in each flight. Specifically, peritoneal macrophage spontaneous secretion of tumor necrosis factor-α occurred in the first but not in the second flight. A significant monocytopenia and lymphocytopenia were detected in the second but not in the first flight. The second mission produced bone changes more consistent with past spaceflight investigations. PEG-IL-2 did not appear to be beneficial; however, this was mostly due to the lack of spaceflight effects. These studies reflect the difficulty in reproducing experimental models by using current space shuttle conditions.


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